"... Simulated dopamine strongly enhanced high, delay-type activity but not low, spontaneous activity in the model network. Furthermore the strength of an afferent stimulation needed to disrupt delay-type activity increased with the magnitude of the dopamine-induced shifts in network parameters, making the currently active representation much more stable. Stability could be increased by dopamine-induced enhancements of the persistent Na(+) and N-methyl-D-aspartate (NMDA) conductances. Stability also was enhanced by a reduction in AMPA conductances. The increase in GABA(A) conductances that occurs after stimulation of dopaminergic D1 receptors was necessary in this context to prevent uncontrolled, spontaneous switches into high-activity states (i.e., spontaneous activation of task-irrelevant representations). In conclusion, the dopamine-induced changes in the biophysical properties of intrinsic ionic and synaptic conductances conjointly acted to highly increase stability of activated representations in PFC networks and at the same time retain control over network behavior and thus preserve its ability to adequately respond to task-related stimuli. ..." See paper and references for more and details.
Model Type: Neuron or other electrically excitable cell
Region(s) or Organism(s): Prefrontal cortex (PFC)
Cell Type(s): Neocortex L5/6 pyramidal GLU cell
Currents: I Na,p; I Na,t; I L high threshold; I K; I Potassium
Model Concept(s): Calcium dynamics
Simulation Environment: NEURON
Implementer(s): Durstewitz, Daniel [daniel.durstewitz at plymouth.ac.uk]
References:
Durstewitz D, Seamans JK, Sejnowski TJ. (2000). Dopamine-mediated stabilization of delay-period activity in a network model of prefrontal cortex. Journal of neurophysiology. 83 [PubMed]